Nuclear translocation of β-catenin correlates with CD44 upregulation in Helicobacter pylori-infected gastric carcinoma
| Autor: | Gopal Udhayakumar, Halagowder Devaraj, Niranjali Devaraj, Venkatraman Jayanthi |
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| Rok vydání: | 2011 |
| Předmět: |
Adult
Male Transcriptional Activation Clinical Biochemistry Molecular Sequence Data Chromosomal translocation Biology Gene mutation medicine.disease_cause Malignant transformation Helicobacter Infections Western blot Stomach Neoplasms medicine CagA Humans Amino Acid Sequence Molecular Biology beta Catenin medicine.diagnostic_test Helicobacter pylori CD44 Carcinoma Cell Biology General Medicine Exons Middle Aged bacterial infections and mycoses biology.organism_classification digestive system diseases Up-Regulation Gene Expression Regulation Neoplastic Protein Transport Cell Transformation Neoplastic Hyaluronan Receptors biology.protein Cancer research Female Carcinogenesis Signal Transduction |
| Zdroj: | Molecular and cellular biochemistry. 357(1-2) |
| ISSN: | 1573-4919 |
| Popis: | Infection with Helicobacter pylori CagA-positive strains is associated with gastric adenocarcinoma. CagA H. pylori activates the β-catenin signal by translocation into nucleus which promotes carcinogenesis. Deregulated accumulation of nuclear β-catenin enhances transcription of β-catenin target genes including CD44 and promotes malignant transformation. The aim of this study was to investigate whether nuclear translocation of β-catenin correlates with CD44 expression in CagA H. pylori-infected gastric carcinoma. To address these issues, we examined 140 gastric biopsy specimens by using immunohistochemical and immunofluorescence staining, Western blot, and mutational analysis of the exon 3 β-catenin gene. The nuclear localization of β-catenin was significantly (χ(2) = 21.175; P < 0.001) increased in advanced gastric carcinoma and also correlated (χ(2) = 22.857; P < 0.001) with the CagA H. pylori positive specimens. We also observed that tyrosine-phosphorylated β-catenin was significantly (χ(2) = 14.207; P < 0.001) increased in samples showing nuclear localization of β-catenin and also it correlated (χ(2) = 43.69; P < 0.03) with the CagA H. pylori positive specimens. Exon 3 β-catenin gene mutation was not detected in H. pylori-infected gastric carcinoma. CD44 up regulation was significantly associated with tyrosine-phosphorylated β-catenin (χ(2) = 22.5; P < 0.001), and this change was closely associated with nuclear translocation of β-catenin (χ(2) = 13.393; P < 0.001) in CagA H. pylori-infected gastric carcinoma. In conclusion, our data suggest that CagA H. pylori infection is responsible for the tyrosine phosphorylation of β-catenin and its nuclear translocation, which upregulates β-catenin target gene CD44 in gastric carcinoma. |
| Databáze: | OpenAIRE |
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